Porcine edema disease often breaks out among young pigs of 4 to 12 weeks old, causes eyelid edema, neurological symptoms and the like and mostly results in death within 24 hours of the onset (NPL 1, Proc. Jpn. Pig Vet. Soc. 2006, 48, 7-13). Its fatality rate is as high as 50 to 90%, and the economic loss is enormous because the productivity decreases due to the recurrence, incomplete development and the like. This disease is caused by Shiga toxin Stx2e produced by Shiga toxin producing Escherichia coli (Shiga toxin producing E. coli, STEC) which is adhered to the intestinal tract. Stx2e is an AB5-type toxin protein containing an A subunit (Stx2eA) having rRNA N-glycosidase activity and a B subunit pentamer (Stx2eB) having a capability of binding to a receptor (globotetraosyl ceramide (Gb4)). It is known that Stx2e which has been taken from the intestinal tract and brought to the surface of a cell such as a vascular endothelial cell by the B subunit sends the A subunit into the cytoplasm of the target cell and inhibits the protein synthesis by the ribosome, thereby inducing the symptoms of edema disease. In Japan, no vaccine for preventing porcine edema disease is commercially available, and although antibiotics are used, the administration after the onset is usually too late. Furthermore, drug-resistant bacteria have been reported, and development of effective preventive method and therapeutic method is desired.
Under these circumstances, methods for effectively preventing porcine edema disease have been investigated. For example, a case of immunization with an Stx2e toxoid has shown an effect of defending against experimental infection (NPL 2, Vet. Microbiol. 1991, 29, 309-318). However, in another report, the onset of edema disease has been observed in some pigs after immunization with a toxoid because detoxification is difficult (NPL 3, Infect. Immun. 1992, 60, 485-90). Moreover, in another example, it is reported that the induction of neutralizing antibodies was confirmed when pigs were immunized with recombinant Stx2e which was detoxified by modifying a part of the amino acid sequence of Stx2eA (NPL 3, Infect. Immun. 1992, 60, 485-90). However, the production of detoxified Stx2e by recombinant E. coli is extremely low, and there are still problems for the practical use.